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Article ; Online: Evaluation of the Antitumor Immune Response Following Photofrin-Based PDT in Combination with the Epigenetic Agent 5-Aza-2'-Deoxycytidine.

Wachowska, Malgorzata / Muchowicz, Angelika / Golab, Jakub

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2451, Page(s) 559–567

Abstract: Photofrin-based photodynamic therapy (PDT) is approved for clinical use by the US Food and Drug Administration and the European Medicines Agency and is among the most widely used photosensitizer for the treatment of cancer. It was broadly reported that ... ...

Abstract	Photofrin-based photodynamic therapy (PDT) is approved for clinical use by the US Food and Drug Administration and the European Medicines Agency and is among the most widely used photosensitizer for the treatment of cancer. It was broadly reported that both the innate and the adaptive arms of immune response can be activated by PDT and play a critical role in the anticancer outcome of this treatment. PDT leads to the induction of acute local inflammation that includes leukocyte infiltration as well as increased activation and production of pro-inflammatory factors and cytokines. These events can lead to the development of systemic and specific antitumor immune response. Combining Photofrin-PDT with the epigenetic agent 5-aza-2'-deoxycytidine results in potentiated antitumor effects in vivo. Understanding the molecular mechanisms underlying this phenomenon would be invaluable for clinical development of this therapeutic approach. This chapter describes a detailed protocol allowing evaluation of specific antitumor immune response induced by PDT.
MeSH term(s)	Decitabine/pharmacology ; Decitabine/therapeutic use ; Dihematoporphyrin Ether/pharmacology ; Dihematoporphyrin Ether/therapeutic use ; Epigenesis, Genetic ; Immunity ; Photochemotherapy ; United States
Chemical Substances	Decitabine (776B62CQ27) ; Dihematoporphyrin Ether (97067-70-4)
Language	English
Publishing date	2022-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2099-1_27
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Article ; Online: The role of CD71

Grzywa, Tomasz M / Nowis, Dominika / Golab, Jakub

Pharmacology & therapeutics

2021 Volume 228, Page(s) 107927

Abstract: Complex regulation of the immune response is necessary to support effective defense of an organism against hostile invaders and to maintain tolerance to harmless microorganisms and autoantigens. Recent studies revealed previously unappreciated roles of ... ...

Abstract	Complex regulation of the immune response is necessary to support effective defense of an organism against hostile invaders and to maintain tolerance to harmless microorganisms and autoantigens. Recent studies revealed previously unappreciated roles of CD71
MeSH term(s)	Antigens, CD/physiology ; COVID-19 ; Erythroid Cells/metabolism ; Humans ; Immunity/physiology ; Receptors, Transferrin/physiology
Chemical Substances	Antigens, CD ; CD71 antigen ; Receptors, Transferrin
Language	English
Publishing date	2021-06-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2021.107927
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Article ; Online: Corrigendum to "The role of CD71+ erythroid cells in the regulation of the immune response" [Pharmacology & Therapeutics 228 (2021) 107927].

Grzywa, Tomasz M / Nowis, Dominika / Golab, Jakub

Pharmacology & therapeutics

2021 Volume 234, Page(s) 108034

Language	English
Publishing date	2021-11-22
Publishing country	England
Document type	Published Erratum
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2021.108034
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Article ; Online: Can Developments in Tissue Optical Clearing Aid Super-Resolution Microscopy Imaging?

Matryba, Paweł / Łukasiewicz, Kacper / Pawłowska, Monika / Tomczuk, Jacek / Gołąb, Jakub

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: The rapid development of super-resolution microscopy (SRM) techniques opens new avenues to examine cell and tissue details at a nanometer scale. Due to compatibility with specific labelling approaches, in vivo imaging and the relative ease of sample ... ...

Abstract	The rapid development of super-resolution microscopy (SRM) techniques opens new avenues to examine cell and tissue details at a nanometer scale. Due to compatibility with specific labelling approaches, in vivo imaging and the relative ease of sample preparation, SRM appears to be a valuable alternative to laborious electron microscopy techniques. SRM, however, is not free from drawbacks, with the rapid quenching of the fluorescence signal, sensitivity to spherical aberrations and light scattering that typically limits imaging depth up to few micrometers being the most pronounced ones. Recently presented and robustly optimized sets of tissue optical clearing (TOC) techniques turn biological specimens transparent, which greatly increases the tissue thickness that is available for imaging without loss of resolution. Hence, SRM and TOC are naturally synergistic techniques, and a proper combination of these might promptly reveal the three-dimensional structure of entire organs with nanometer resolution. As such, an effort to introduce large-scale volumetric SRM has already started; in this review, we discuss TOC approaches that might be favorable during the preparation of SRM samples. Thus, special emphasis is put on TOC methods that enhance the preservation of fluorescence intensity, offer the homogenous distribution of molecular probes, and vastly decrease spherical aberrations. Finally, we review examples of studies in which both SRM and TOC were successfully applied to study biological systems.
MeSH term(s)	Animals ; Brain/diagnostic imaging ; Fluorescence ; Fluorescent Dyes/chemistry ; Humans ; Image Processing, Computer-Assisted/methods ; Microscopy/methods ; Molecular Probes/chemistry ; Optical Imaging/methods ; Tissue Fixation/methods
Chemical Substances	Fluorescent Dyes ; Molecular Probes
Language	English
Publishing date	2021-06-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22136730
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Article: Tumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development.

Grzywa, Tomasz M / Justyniarska, Magdalena / Nowis, Dominika / Golab, Jakub

Cancers

2021 Volume 13, Issue 4

Abstract: Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune ... ...

Abstract	Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune surveillance results from multiple independent mechanisms. Recent studies revealed that besides well-described myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs) or regulatory T-cells (Tregs), erythroid progenitor cells (EPCs) play an important role in the regulation of immune response and tumor progression. EPCs are immature erythroid cells that differentiate into oxygen-transporting red blood cells. They expand in the extramedullary sites, including the spleen, as well as infiltrate tumors. EPCs in cancer produce reactive oxygen species (ROS), transforming growth factor β (TGF-β), interleukin-10 (IL-10) and express programmed death-ligand 1 (PD-L1) and potently suppress T-cells. Thus, EPCs regulate antitumor, antiviral, and antimicrobial immunity, leading to immune suppression. Moreover, EPCs promote tumor growth by the secretion of growth factors, including artemin. The expansion of EPCs in cancer is an effect of the dysregulation of erythropoiesis, leading to the differentiation arrest and enrichment of early-stage EPCs. Therefore, anemia treatment, targeting ineffective erythropoiesis, and the promotion of EPC differentiation are promising strategies to reduce cancer-induced immunosuppression and the tumor-promoting effects of EPCs.
Language	English
Publishing date	2021-02-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13040870
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Article: Arginase Inhibition Mitigates Bortezomib-Exacerbated Cardiotoxicity in Multiple Myeloma.

Paterek, Aleksandra / Oknińska, Marta / Pilch, Zofia / Sosnowska, Anna / Ramji, Kavita / Mackiewicz, Urszula / Golab, Jakub / Nowis, Dominika / Mączewski, Michał

Cancers

2023 Volume 15, Issue 7

Abstract: Background: Multiple myeloma (MM) is associated with increased cardiovascular morbidity and mortality, while MM therapies also result in adverse cardiac effects. Endothelial dysfunction and impaired nitric oxide (NO) pathway is their possible mediator.!# ...

Abstract	Background: Multiple myeloma (MM) is associated with increased cardiovascular morbidity and mortality, while MM therapies also result in adverse cardiac effects. Endothelial dysfunction and impaired nitric oxide (NO) pathway is their possible mediator. Objective: Since MM is associated with increased arginase expression, resulting in the consumption of ʟ-arginine, precursor for NO synthesis, our aim was to test if cardiotoxicity mediated by MM and MM therapeutic, bortezomib (a proteasome inhibitor), can be ameliorated by an arginase inhibitor through improved endothelial function. Methods: We used a mouse VĸMYC model of non-light chain MM. Cardiac function was assessed by echocardiography. Results:* MM resulted in progressive left ventricular (LV) systolic dysfunction, and bortezomib exacerbated this effect, leading to significant impairment of LV performance. An arginase inhibitor, OAT-1746, protected the heart against bortezomib- or MM-induced toxicity but did not completely prevent the effects of the MM+bortezomib combination. MM was associated with improved endothelial function (assessed as NO production) vs. healthy controls, while bortezomib did not affect it. OAT-1746 improved endothelial function only in healthy mice. NO plasma concentration was increased by OAT-1746 but was not affected by MM or bortezomib. Conclusions: Bortezomib exacerbates MM-mediated LV systolic dysfunction in a mouse model of MM, while an arginase inhibitor partially prevents it. Endothelium does not mediate either these adverse or beneficial effects. This suggests that proteasome inhibitors should be used with caution in patients with advanced myeloma, where the summation of cardiotoxicity could be expected. Therapies aimed at the NO pathway, in particular arginase inhibitors, could offer promise in the prevention/treatment of cardiotoxicity in MM.
Language	English
Publishing date	2023-04-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15072191
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Article: Extracellular vesicles released by ovarian carcinoma contain arginase 1 that mitigates antitumor immune response.

Sosnowska, Anna / Czystowska-Kuzmicz, Malgorzata / Golab, Jakub

Oncoimmunology

2019 Volume 8, Issue 11, Page(s) e1655370

Abstract: Expression of arginase-1 (ARG1) is an immunosuppressive feature of tumor microenvironment that leads to depletion of ʟ-arginine, a nutrient required for T-cells expansion. Ovarian carcinoma cells release extracellular vesicles carrying enzymatically ... ...

Abstract	Expression of arginase-1 (ARG1) is an immunosuppressive feature of tumor microenvironment that leads to depletion of ʟ-arginine, a nutrient required for T-cells expansion. Ovarian carcinoma cells release extracellular vesicles carrying enzymatically active ARG1, that contributes to local and systemic immune suppression, which can be restored by ARG inhibitor.
Language	English
Publishing date	2019-08-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2645309-5
ISSN	2162-402X ; 2162-4011
ISSN (online)	2162-402X
ISSN	2162-4011
DOI	10.1080/2162402X.2019.1655370
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Article: SARS-CoV-2 and its ORF3a, E and M viroporins activate inflammasome in human macrophages and induce of IL-1α in pulmonary epithelial and endothelial cells.

Ambrożek-Latecka, Magdalena / Kozlowski, Piotr / Hoser, Grażyna / Bandyszewska, Magdalena / Hanusek, Karolina / Nowis, Dominika / Gołąb, Jakub / Grzanka, Małgorzata / Piekiełko-Witkowska, Agnieszka / Schulz, Luise / Hornung, Franziska / Deinhardt-Emmer, Stefanie / Kozlowska, Ewa / Skirecki, Tomasz

Cell death discovery

2024 Volume 10, Issue 1, Page(s) 191

Abstract: Inflammasome assembly is a potent mechanism responsible for the host protection against pathogens, including viruses. When compromised, it can allow viral replication, while when disrupted, it can perpetuate pathological responses by IL-1 signaling and ... ...

Abstract	Inflammasome assembly is a potent mechanism responsible for the host protection against pathogens, including viruses. When compromised, it can allow viral replication, while when disrupted, it can perpetuate pathological responses by IL-1 signaling and pyroptotic cell death. SARS-CoV-2 infection was shown to activate inflammasome in the lungs of COVID-19 patients, however, potential mechanisms responsible for this response are not fully elucidated. In this study, we investigated the effects of ORF3a, E and M SARS-CoV-2 viroporins in the inflammasome activation in major populations of alveolar sentinel cells: macrophages, epithelial and endothelial cells. We demonstrated that each viroporin is capable of activation of the inflammasome in macrophages to trigger pyroptosis-like cell death and IL-1α release from epithelial and endothelial cells. Small molecule NLRP3 inflammasome inhibitors reduced IL-1 release but weakly affected the pyroptosis. Importantly, we discovered that while SARS-CoV-2 could not infect the pulmonary microvascular endothelial cells it induced IL-1α and IL-33 release. Together, these findings highlight the essential role of macrophages as the major inflammasome-activating cell population in the lungs and point to endothelial cell expressed IL-1α as a potential novel component driving the pulmonary immunothromobosis in COVID-19.
Language	English
Publishing date	2024-04-25
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-024-01966-9
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Article: Cancer stem cells in haematological malignancies.

Zagozdzon, Radoslaw / Golab, Jakub

Contemporary oncology (Poznan, Poland)

2015 Volume 19, Issue 1A, Page(s) A1–6

Abstract: At least several types of human haematological malignancies can now be seen as 'stem-cell diseases'. The best-studied in this context is acute myeloid leukaemia (AML). It has been shown that these diseases are driven by a pool of 'leukaemia stem cells ( ... ...

Abstract	At least several types of human haematological malignancies can now be seen as 'stem-cell diseases'. The best-studied in this context is acute myeloid leukaemia (AML). It has been shown that these diseases are driven by a pool of 'leukaemia stem cells (LSC)', which remain in the quiescent state, have the capacity to survive and self-renew, and are responsible for the recurrence of cancer after classical chemotherapy. It has been understood that LSC must be eliminated in order to cure patients suffering from haematological cancers. Recent advances in LSC research have allowed for description of LSC phenotype and identification of potential targets for anti-LSC therapies. This concise review summarises the current view on LSC biology and targeted approaches against LSC.
Language	English
Publishing date	2015-01-29
Publishing country	Poland
Document type	Journal Article ; Review
ISSN	1428-2526
ISSN	1428-2526
DOI	10.5114/wo.2014.47127
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Article ; Online: Inhibition of Macrophage-Specific CHIT1 as an Approach to Treat Airway Remodeling in Severe Asthma.

Sklepkiewicz, Piotr / Dymek, Barbara / Mlacki, Michal / Zagozdzon, Agnieszka / Salamon, Magdalena / Siwińska, Anna Maria / Mazurkiewicz, Marcin Piotr / de Souza Xavier Costa, Natalia / Mazur, Marzena / Mauad, Thais / Gołębiowski, Adam / Dzwonek, Karolina / Gołąb, Jakub / Zasłona, Zbigniew

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: Chitotriosidase (CHIT1) is an enzyme produced by macrophages that regulates their differentiation and polarization. Lung macrophages have been implicated in asthma development; therefore, we asked whether pharmacological inhibition of macrophage-specific ...

Abstract	Chitotriosidase (CHIT1) is an enzyme produced by macrophages that regulates their differentiation and polarization. Lung macrophages have been implicated in asthma development; therefore, we asked whether pharmacological inhibition of macrophage-specific CHIT1 would have beneficial effects in asthma, as it has been shown previously in other lung disorders. CHIT1 expression was evaluated in the lung tissues of deceased individuals with severe, uncontrolled, steroid-naïve asthma. OATD-01, a chitinase inhibitor, was tested in a 7-week-long house dust mite (HDM) murine model of chronic asthma characterized by accumulation of CHIT1-expressing macrophages. CHIT1 is a dominant chitinase activated in fibrotic areas of the lungs of individuals with fatal asthma. OATD-01 given in a therapeutic treatment regimen inhibited both inflammatory and airway remodeling features of asthma in the HDM model. These changes were accompanied by a significant and dose-dependent decrease in chitinolytic activity in BAL fluid and plasma, confirming in vivo target engagement. Both IL-13 expression and TGFβ1 levels in BAL fluid were decreased and a significant reduction in subepithelial airway fibrosis and airway wall thickness was observed. These results suggest that pharmacological chitinase inhibition offers protection against the development of fibrotic airway remodeling in severe asthma.
MeSH term(s)	Animals ; Humans ; Mice ; Airway Remodeling/drug effects ; Asthma/pathology ; Asthma/therapy ; Chitinases/antagonists & inhibitors ; Disease Models, Animal ; Lung/metabolism ; Macrophages/enzymology ; Pyroglyphidae/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Chitinases (EC 3.2.1.14) ; chitotriosidase (EC 3.2.1.-) ; OATD-01 ; Protein Kinase Inhibitors
Language	English
Publishing date	2023-03-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054719
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